Test 3: Wk 11: 8 Neural Control of Breathing - Puri Flashcards

1
Q

Dyspnea is the feeling of

A

being short of breath, or the unpleasant conscious

awareness of difficulty in breathing.

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2
Q

when arterial PaO2 falls or PaCO2 rises from breath holding, asphyxia,
or pulmonary disease, dyspnea leads to

A

efforts to increase ventilation and thus to restore arterial blood gas levels to normal

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3
Q

What causes dyspnea when blood gasses are normal

A

increased airway resistance

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4
Q

mechanical event for inspiration

A

contraction of diaphragm

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5
Q

neural event for inspiration

A

firing of phrenic motoneurons

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6
Q

where are phrenic motor neurons located

A

within the ventral horn of the cervical spinal cord c3-c5

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7
Q

mechanical event for expiration

A

relaxation of diaphragm and recoil of lungs

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8
Q

neural event for expiration

A

phrenic motoneurons stop firing

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9
Q

rate of respiration is dependent on

A

the interval between bursts of phrenic nerve action potentials

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10
Q

tidal volume is determined by

A

the strength of the diaphragm contraction which is determined by the number of phrenic motor units recruited

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11
Q

— controls the act of breathing

A

the medullary pattern generator

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12
Q

below level IV

A

all breathing stops

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13
Q

Below level I

A

all breathing intact

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14
Q

cut at level III (btwn pons and medulla)

A

tidal volume increased and apneustic breathing starts

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15
Q

Dorsal Respiratory Group (DRG are — neurons in the —

A

Inspiratory neurons in the ventrolateral nucleus of the tractus solitarius (NTS)

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16
Q

The tractus solitarius project primarily to the — for —

A

contralateral phrenic motoneurons for passive inspiration and expiration

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17
Q

expiratory neurons in the nuclease retroambigualis

A

Ventral Respiratory Group (VRG)

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18
Q

the nucleus retroambigualis project to — and — for —

A

contralaterally to abdominal and intercostal muscles.

Primarily for forced expiration

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19
Q

Bötzinger and Pre-Bötzinger complexes contain

A

pacemaker cells

for automatic generation of respiratory rhythm

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20
Q

Inspiratory “Ramp” Signal:

A

The nervous signal that is transmitted to the inspiratory

muscles, mainly the diaphragm via the phrenic nerve

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21
Q

how does ramp signal work

A

not an instantaneous burst of action potentials. Instead, it begins weakly and increases steadily in a ramp manner for about 2 seconds in normal respiration. Then it ceases abruptly for approximately the next 3 seconds, which turns off the excitation of the diaphragm and allows elastic recoil of the lungs and the chest wall to cause expiration.

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22
Q

advantage of ramp signal

A

causes a steady increase in the volume of

the lungs during inspiration, rather than inspiratory gasps

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23
Q

The — controls the “switch-off” point of the inspiratory ramp, thus
controlling the duration of the filling phase of the lung cycle.

A

pneumotaxic center

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24
Q

The function of the pneumotaxic center is primarily —

A

to limit inspiration

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25
Q

apneustic breathing

A

prolonged inspiratory efforts interrupted by

occasional expirations

26
Q

opiates inhibit

A

the central pattern generator

27
Q

opiates and benzos cause

A

respiratory depression

28
Q

Excitatory amino acids, —, activated — receptors

A

glutamate, NMDA

29
Q

Inhibitory neurotransmitters include — and —

A

glycine and γ-aminobutyric acid (GABA)

30
Q

Benzodiazepines exert their
effect by binding directly to — increasing the inhibitory effect
of —

A

GABAA

endogenous GABA.

31
Q

Peripheral chemoreceptors activate the CPG via

A

glutamate-releasing neurons.

32
Q

Central chemoreceptors activate the CPG via

A

acetylcholine-releasing neurons.

33
Q

peripheral chemoreceptors located in

A

carotid bodies and aortic bodies

34
Q

Peripheral chemoreceptors carotid bodies afferent pathway

A

Glossopharyngeal Nerve CN IX

35
Q

Peripheral Chemoreceptor aortic bodies afferent pathway

A

Vagus Nerve CN X

36
Q

peripheral chemoreceptors are exposed to

A

arterial blood

37
Q

peripheral chemoreceptors respond to (3)

A

⬇ PaO2
⬆ PaCO2
⬇ pH

38
Q

peripheral chemoreceptors pH detected by — only

A

carotid

39
Q

central chemoreceptors location

A

ventrolateral medulla near exits of CN IX and X

40
Q

central chemoreceptors chemical stimuli

A

increased medullary extracellular and CSF H+ resulting from ⬆ PaCO2

41
Q

central chemoreceptors are not stimulated by

A

decreased PO2 (hypoxia)

42
Q

central chemoreceptors respond to changes in — H+ concentration

A

CSF

43
Q

— ions directly activated central chemoreceptors

A

H+

44
Q

— does not directly act on central chemoreceptors

A

CO2

45
Q

normal drive for ventilation during acute hypercapnia

A

increased PaCO2

46
Q

— are acute regulators of day to day breathing and respond to changes in —

A

central chemoreceptors

CO2

47
Q

defect in central chemoreceptors

A

they “reset” if changes in CO2 are prolonged, like baroreceptors

48
Q

shift in sensitivity to PaCO2 is exaggerated in

A

metabolic acidosis

49
Q

Chemical control of breathing in pts with chronic hypercapnia

A

central chemoreceptors adapt to prolonged elevated PaCO2 and are no longer the central regulator
pts with COPD have decreased O2 which will activate peripheral chemoreceptors

50
Q

the main stimulus to breathe in chronic hypercapnia is

A

Hypoxic Drive

51
Q

oxygen induced hypoventilation

A

administration of high concentrations of O2 to a person with chronic hypercapnia will increased their Pa)2 and knock out their hypoxic drive

52
Q

for hypoxic drive to kick in PaO2 must drop below

A

60mmHg

53
Q

when PaO2 decreases to threshold levels the ventilatory response is mediated solely by

A

carotid chemoreceptors

54
Q

— does not stimulate the central chemoreceptors

A

decreased PaO2

55
Q

synergistic effect on ventilation when

A

increased PaCO2 accompanies decreased PaO2

56
Q

pulmonary stretch receptors act to

A

terminate inspiration and decrease respiratory rate by increasing expiratory time

57
Q

Hering-Breuer Inflation Reflex mediated by

A

impulses traveling in the vagus nerve

58
Q

Hering-Breuer Inflation Reflex originates in slowly adapting stretch receptors located within

A

smooth muscle of large bronchi and small bronchioles

59
Q

most stretch receptors fire during

A

tidal breathing

60
Q

deep breaths — Liter(s) are sufficiently large enough to trigger stretch reflex

A

1 liter

61
Q

Activation of rapidly adapting receptors in the trachea cause

A

cough, bronchoconstriction, and mucus secretion